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REPORT ON THE SELECTION OF PRIORITY CHEMICALS TO BIOMONITOR IN MICHIGAN RESIDENTS Presented to the Michigan Environmental Science Board by the Human Biomonitoring Planning Grant Committee: Frances Pouch Downes, PhD Dave Wade, PhD John Riebow, PhD Lorri Cameron, PhD Paul Loconto, PhD Julie Wirth, PhD, MS Michigan Department of Community Health Bureau of Laboratories Bureau of Epidemiology Prepared by Julie Wirth April 24, 2003

TABLE OF CONTENTS Introduction…………………………………………………………………………………………………... 1 Stakeholders………………………………………………………………………………………………... 1 Criteria for chemical selection……………………………………………………………………………... 2 Reviews of priority chemicals……………………………………………………………………………… 3 Heavy metals………………………………………………....................................................... 3 Methyl mercury…………………………………………………………………………… 3 Lead……………………………………………………………………………………….. 6 Arsenic…………………………………………………………………………………..... 8 Cadmium…………………………………………………………………………..…….. 11 Manganese………………………………………..…………………………….……..… 13 Chemicals………………………………………………………………………………….……… 15 PCBs……………………………………………………………………………………… 15 PBBs……………………………………………………………………………………… 18 Dioxins and furans………………………………………………………………………. 20 Organochlorine pesticides………………………….................................................. 25 Dichlorodiphenyltrichloroethane………..................................................... 25 Organophosphate pesticides………………………………………………..……….… 28 Benzene………………………………………………………………………………….. 47 Emerging chemicals…………………………………………………………………….………... 33 PFOS and PFOA……………………………………………………………..……….… 33 Phthalates………………………………………………………………………………... 35 Polybrominated diphenyls ethers……………………………………………………… 37 Appendix………………………………………………………………………………………………….…. Organizations…………………………………………………………………………………..…. People Interviewed………………………………………………………………………..……… Stakeholders Groups…………………………………….…………………………………….… Implementation Group………………………………………………………………………….... Priority Chemicals………………………………………………………………………………... Comparative Chemical List……………………………………………………………………….

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INTRODUCTION The following report includes a description of the process we followed to compile our list of chemicals in the Michigan environment that warrant human biomonitoring, as well as the list itself and our rationale for selecting individual chemicals. Biomonitoring is the measurement of environmental chemicals in the human body, specifically in blood, urine, serum, saliva, or tissues, as a means to evaluate the body burden or the internal, delivered or biologically effective dose of a chemical exposure. More specifically, biomonitoring is a method of determining exposure to chemicals found in the environment that have come in contact with a body surface, such as the respiratory tract, gastrointestinal tract or skin and have been absorbed into the body and into the circulation. The first two sections, Stakeholders and Selection Criteria, describe the process we used to select the chemicals. The remaining sections review the scientific literature on each chemical as it pertains to the Selection Criteria. STAKEHOLDERS To obtain a statewide overview on the health issues associated with exposure to environmental contaminants, we chose to interview individuals from a variety of organizations across the state of Michigan. We began by listing the organizations, both local and national, that would have an interest in issues relating to health and the environment (see List of Organizations in the Appendix). From this list we identified individuals from these organizations to contact. At the same time, we constructed a questionnaire to be administered to these individuals, whom we considered potential stakeholders, soliciting their opinion as to which chemicals in the Michigan environment posed the greatest potential danger to the health of Michigan residents. We first interviewed employees of the State of Michigan who were in positions that dealt with public health issues involving environmental chemicals. For example, we interviewed the head of the Childhood Lead Program and the Deputy Director of the Department of Community Health. These early interviews lead us to modify the questionnaire from a fairly structured set of questions to four open-ended questions to allow the individuals to expand on areas that concerned them: 1. 2. 3. 4.

Which chemicals should be biomonitored and why? What use will the information we collect have and for whom? Would you be willing to work with us as we develop a biomonitoring plan for Michigan? Can you suggest anyone else who might be interested in working with us?

Following these interviews, we contacted individuals from the organizations outside of state government (see List of People Interviewed in the Appendix) as well as those suggested by the interviewees. At the conclusion of these interviews, we had a preliminary list of chemicals of concern for Michigan residents. This list closely matched regional lists of chemicals of concern published by State-related and Federal agencies (see Comparative Chemical List in the Appendix). From our lists of internal and external interviewees who indicated an interested in continuing to work with us on developing a biomontoring plan for Michigan, we selected a group of potential stakeholders. The potential stakeholders naturally fell into two groups: those with expertise in clinical laboratory management and analyses (Analytical Chemist Group) and those with other areas of expertise (Implementation Planning Group) (see the Appendix for a list of the Stakeholders Groups). All individuals were sent a letter of invitation to attend 3-4 meetings to be held at the Michigan Institute for Public Health (MPHI), Okemos, MI. Those who sent an email reply to the letter indicating that they wanted to participate became Stakeholders. Since we invited individuals with diverse backgrounds and wanted to make maximum use of their distinct perspectives, we hired a facilitator, Michelle Napier Dunnings, from Project Innovations, Detroit, MI. The core members of the Biomonitoring Planning Group (Frances Pouch Downes, David R Wade, John Riebow, Lori Cameron, Paul Loconto and Julie Wirth) initially met with Ms Napier Dunnings to acquaint her with the background on the Planning Grant and to develop the overall goals for the Stakeholders meetings. At the end of the meetings, we hoped to have a set of criteria for selection of chemicals to biomonitor, a list of chemicals to biomonitor and the justification for selecting

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each chemical. Before each meeting, Ms Napier-Dunnings and the Core Group meet to determine the Desired Outcomes of each meeting and to decide on material to provide to the Stakeholders prior to or at the time of the meeting. Since the meetings were scheduled two weeks apart, we also meet immediately after each meeting to discuss the outcomes, assess progress and decide on the format for the following meeting. The Agendas in brief and formats for each meeting were as follows: Meeting #1 – Possibilities; both groups met as one Meeting #2 - Priorities; the two groups met separately with separate, but related Agendas Meeting #3 – Setting Directions; both groups met as one. The Stakeholders meetings accomplished the desired results: we have a list of criteria for chemical selection (see below for Selection Criteria) and a priority list of chemicals to biomonitor, including their ranking based on the criteria, and the status of the MDCH laboratory capacity to biomonitor them (see Priority Chemicals List in the Appendix). Lessons learned: we found it was extremely useful to have a highly skilled facilitator to moderate the discussion, to ensure all viewpoints were heard and taken into consideration, and to ensure that the overall goals were met. The Analytical Chemist Group has continued to provide opinions on various aspects of sample preparation as well as a proposed integrated scheme for laboratory biomonitoring. Their input continues to aid us as we prepare our final Biomonitoring Plan and the Implementation Grant. CRITERIA FOR CHEMICAL SELECTION The criteria for selecting the chemicals to biomonitor were arrived at through extensive discussion by members of both the Analytical Chemist Group and the Strategic Implementation Group during the second meeting. Highest consideration was given to chemicals associated with known or potential adverse health effects, with chemicals with known adverse human health effects given the highest numerical ranking. Recognizing, however, that several chemicals under consideration have not yet been investigated in epidemiological studies to evaluate their effects on human health, two other sub categories were created. Chemicals for which experimental animal or in vitro cell culture data indicated potential for adverse human health effects received a lower numerical score, while those with chemical structures similar to other chemicals with known adverse human health effects received the lowest score in this category. The second criterion for chemical selection was the probability of human exposure. Within that heading, chemicals for which significant human exposure in terms of number of potentially exposed individuals has been documented were given the highest score. Those chemicals with more limited human exposure, for example chemical exposures associated with specific activities, but which were shown to bio-accumulate, received a lower numerical rank. The third criterion, seriousness of health effect, was based on the length of life affected by the exposure and the severity of the effect, i.e. was it life threatening. Chemicals causing human cancer were highly ranked in this category. A chemical that affected the fetus via an in utero exposure would have a greater or more serious effect than a chemical exposure occurring later in life and was ranked higher. An adverse effect that was passed on from one generation to the next also received a somewhat lower score. In most instances, the distinction was used for chemicals that had not been examined in human epidemiological studies but had been tested in experimental animal studies. The numerical rankings were as follows: Health Effect (range 0 to 5.0) • Human health effect: 5.0 • Animal or other health effect: 4.5 • Structural similarities to chemical with know adverse human health effect: 4.0 • None of the above: 0 Probability of Exposure (range 0 to 3.5) • Significant exposure: 3.5

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Bio-accumulation: 3.0 None of the above: 0

Seriousness of Health Effect (range 0 to 2.5) • Effect occurs early in life (in utero): 2.5 • Cancer: 2.5 • Multigenerational: 2.0 • Early in life and multigenerational: 4.5 • Other: 1.5 • None of the above: 0 REVIEW OF PRIORITY CHEMICALS The complete table of the Priority Chemicals, which includes their ranking based on the chemical selection criteria described above, and the laboratory capacity for their analysis can be found in the Appendix. Below we provide the scientific rationale for their inclusion in the Priority Chemical List. HEAVY METALS The MDCH Analytical Chemistry Laboratory has the capacity to measure a panel of metals from a single sample, which enabled us to perform the analysis for several heavy metals that individually met the selection criteria without additional cost. •

METHYLMERCURY

Background Inorganic mercury exists naturally in the environment and finds its way into the air through both natural processes and human activities. Power plants that burn fossil fuels, particularly coal, generate the greatest amount of mercury emissions. In Michigan, inorganic mercury in the atmosphere is deposited into the Great Lakes and into many of the freshwater inland lakes. In these waterbodies, it is converted to methylmercury, its most toxic form, by aquatic organisms. Methylmercury is then taken up by fish and bioaccumulates in the aquatic food chain biomagnifying to tens of thousands to millions of times the concentration found in water (EPA, 1997). Probability of Exposure: Consumption of mercury-contaminated food is the major source of methylmercury exposure (US EPA, 1999). In the Great Lakes region consumption of sport-caught fish is the greatest risk factor for methylmercury exposure (Zabik et al., 1995; DeVault et al., 2996). Approximately 2 million Michigan residents fish in Michigan waters each year and are potentially exposed, and often ignore fish consumption advisories (Johnson and De Rosa, 1999). Methylmercury can accumulate if consumed at a greater rate than that excreted. It binds strongly to sulfhydryl groups in tissues and accumulates to higher concentrations in brain, muscle and kidney (National Academy of Sciences, 2000). Methylmercury easily crosses the blood-brain barrier where it is converted to inorganic mercury, which has a long half-life in brain tissue measured in years (Clarkson 1997; Davis et al. 1994; Pedersen et al. 1999). Total blood level of mercury is a good indicator of methylmercury exposure, but also includes small amounts of inorganic mercury (National Academy of Sciences, 2000). The current U.S. Environmental Protection Agency (U.S. EPA) recommended reference dose (RfD) for blood mercury levels is 5.8 ug/L (Mahaffey and Rice, 1998). A recent study from an internal medicine practice in California with an excessive number of patients with neurological problems, evaluated all patients attending the clinic in a 1-year period for excess mercury using the current RfD (Hightower and Moore, 2003). Mercury levels ranged from 2.0 to 89.5 µg/L for 89 subjects. The mean for female patients was 15 ug/L and for men, 23 ug/L. A substantial fraction of patients had diets high in fish consumption; of

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these, 89% had blood mercury levels exceeding the maximum level recommended by the U.S. EPA (5.8 ug/L). The mean level for women in this survey was 10 times that of mercury levels found in a recent population survey by the U.S. CDC (CDC, 1999) of 1.3 ug/l. Some children’s levels were > 40 times the national mean. These results suggest that high fish consumption may pose a risk for exposure to methyl mercury levels above the current standard and that these levels may be associated with neurological problems. Another recent report using data from the 1999-2000 National Health and Nutrition Examination Survey (NHANES) found that approximately 8% of the women had blood mercury levels above the US EPA RfD (Schober et al., 2003). Of concern was the finding that the mean mercury levels were almost 4-fold higher among women who ate 3 or more servings of fish in the past 30 days compared with women who reported eating no fish during that period. These results also suggest a possible association between fish consumption and blood levels of methyl mercury above the US EPA current standard. Health Effects: Public health concerns about methylmercury in edible fish began in 1969 when fish from Lake St. Clair bordering Michigan were found to have high levels. Since then many studies have shown that methylmercury is highly toxic and causes adverse effects in several organ systems through the life span of humans and animals. The major target for methylmercury is the central nervous system (US EPA, 2002; ATSDR, 1999). Studies of populations highly exposed to methylmercury, such as those in Japan (Harada et al., 1995) and Iraq (Bakir et al, 1973), have shown that methylmercury adversely affects cognitive, motor and sensory functions. A study on fish consumption in Finland found significant associations between mercury levels and cardiovascular disease (Salonen et al, 1995) and atherosclerosis (Salonen et a., 2000). Mercury effects on blood pressure regulation, heart rate variability and heart disease have also been reported (Frustaci et al., 1997). Severity of Effects Of particular concern are the effects of methylmercury on neurodevelopment. Both the Japan and Iraq outbreaks provided evidence that severe brain damage can occur from high prenatal methylmercury exposure (Bakir et al, 1973) as well as from mothers with mild symptoms (Harada et al., 1995). Subsequent studies on chronic low-dose prenatal methylcercury exposure from maternal consumption of fish have found subtle end points of neurotoxicity in children, including poor performance on neurobehavioral tests, particularly on tests of attention, fine-motor function, language, visual-spatial abilities and verbal memory (Meyers et al., 1995; Marsh et al., 1987). The National Academy of Sciences report on the Toxicological Effects of Methylmercury (National Academy of Sciences, 2000) concluded that perinatal exposure methylmercury is likely to result in an increase in the number of children with learning problems that may require remedial classes or special education. Of particular concern for Michigan residents is the finding that high fish consumers have mercury levels close to those found in young children exposed in utero who have developed neurological problems (Davidson et al., 1998; Grandjean et al., 1999). Why methylmercury should be biomonitored in Michigan: • Methylmercury is a neurotoxin and the developing fetus is most sensitive to its effects • Methylmercury is found in high levels in Michigan sport-caught fish • Michigan has a significant number of sport fish consumers • Methylmercury levels in MI sport fish consumers may reach levels where adverse effects occur for pregnant women References 1. Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological Profile for Mercury [Update]. Atlanta, GA: Agency for Toxic Substances and Disease Registry; US Department of Health and Human Services; 1999. 2. Airey D. Total mercury concentrations in human hair from 13 countries in relation to fish consumption and location. Sci Total Environ 1983;31:157-182.

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3. Airey D. Mercury in human hair due to environment and diet: a review. Environ Health Perspect 1983;52:303-16. 4. CDC. First National Report on Human Exposure to Environmental Chemicals Results: Mercury. 1999. U.S. Centers for Disease Control and Prevention. 5. Clarkson T. An outbreak of mercury poisoning due to consumption of contaminated grain. Fed Proc 1975;34:2395-2399. 6. Davidson PW, Myers GJ, Cox C et al. Effects of prenatal and postnatal methylmercury exposure from fish consumption on neurodevelopment: outcomes at 66 months of age in the Seychelles Child Development Study. JAMA 1998;280:701-707. 7. Davis LE, Kornfeld M, Mooney HS, Fiedler KJ, Haaland KY, Orrison WW, et al. Methylmercury poisoning: long-term clinical, radiological, toxicological, and pathological studies of an affected family. Ann Neurol 1994;35:680-688. 8. DeVault DS, Hesselberg R, Rodgers PW, Feist TJ. Contaminant Trends in Lake Trout and Walleye from the Laurentian Great Lakes. J. Great lakes Res. 1996;22:884-895. 9. Frustaci A, Magnavita N, Chimenti C, Caldarulo M, Sabbioni E, Pietra R, et al. Marked elevation of myocardial trace elements in idiopathic dilated cardiomyopathy compared with secondary cardiac dysfunction. J Am Coll Cardiol 1999;33:1578-1583. 10. Grandjean P, Budtz-Jorgensen RF, White RF et al. Methylmercury exposure in children aged 7 years. Am J Epidemiol 1999;150:301-305. 11. Harada M. Minamata disease: methylmercury poisoning in Japan caused by environmental pollution. Crit Rev Toxicol 25; 1995:1-24. 12. Harris R. H, C. Mercury-measuring and managing the risk. Environment 1978;20:25-36. 13. Hightower JM and Moore D. Mercury levels in high-end consumers of fish. Environ Health Perspect 2003; 111:604-608. 14. Johnson BL HH, De Rosa T. Key Environmental Human Health Issues in the Great Lakes and St. Lawrence River Basins. Environ. Research Section A. 1999;80:S2-S12. 15. Mahaffey KR, and Rice GE. Environmental Protection Agency Office of air Quality Planning and Standards. Mercury Study Report to Congress. Gov’t Reports Announcements and Index (GRA and I), Issue 09.1998. 16. Marsh DO, Clarkson TW, Cox C, Myers GJ, Amin-Zaki L, Al-Tikriti S. Fetal methylmercury poisoning: relationship between concentration in single strands of maternal hair and child effects. Arch Neurol 1987;44:1017-1022. 17. Myers GJ, Davidson PW, Cox C, Shamlaye CF, Tanner MA, Choisy O, Sloane-Reeves J, Marsh DO, Cernichiari E, Cox A, et al. Neurodevelopmental outcomes of Seychellois children sixty-six months after in utero exposure to methylmercury from a maternal fish diet: pilot study. Neurotoxicology 1995;16:639-652. 18. National Academy of Sciences. Toxicological Effects of Methylmercury. Washington, DC: National Academy of Sciences. July 2000. 19. Pedersen MB, Hansen JC, Mulvad G, Pedersen HS, Gregersen M, Danscher G. Mercury accumulations in brains from populations exposed to high and low dietary levels of methylmercury. Int J Circumpolar Health. 1999; 58:96-107. 20. Salonen JT, Seppänen K, Nyyssönen K, Korpela H, Kauhanen J, Kantola M, et al. Intake of mercury from fish, lipid peroxidation, and the risk of myocardial infarction and coronary, cardiovascular, and any death in eastern Finnish men. Circulation 1995;91:645-655. 21. Salonen JT, Seppanen K, Lakka TA, Salonen R, Kaplan GA. Mercury accumulation and accelerated progression of carotid atherosclerosis: a population-based prospective 4-year followup study in men in eastern Finland. Atherosclerosis 2000;148:265-273. 22. Schober SE, Sinks TH, Bolger PM, McDowell, M et al. Blood mercury levels in US children and women of childbearing age, 1999-2000. JAMA 2003;289:1667-1674. 23. US EPA. Mercury Study: Report to Congress, Volume I: Executive Summary. Washington, DC: US Environmental Protection Agency, 1997. 24. US EPA. Office of Water. Mercury Update: Impact on Fish Advisories. Washington, DC: U.S. Environmental Protection Agency. 1999. 25. Zabik ME, Zabik MJ, Booren AM, et al. Pesticides and total polychlorinated biphenyls residues in raw and cooked walleye and white bass harvested from the Great Lakes. Bull Environ Contam Toxicol. 1995;54:396-402.

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LEAD

Background Lead is naturally-occurring element, but is often released into the environment from man-made sources such as mining and smeltering (Pirkle et al, 1998; Juberg, 2000). Lead has been used as an additive in paint and gasoline, and in leaded pipes, solder, crystal, and ceramics (ATSDR, 1999). Natural levels of lead in soil are usually low, but human activities have resulted in substantial increases in lead levels in the environment, especially near mining and smelting sites, near some types of industrial and municipal facilities, and adjacent to highways. Lead particles in the environment can attach to dust and be carried long distances in the air (ATSDR, 1999; Juberg, 2000). Such lead-containing dust is often removed from the air by rain and deposited on surface soil, where it may remain for many years. In addition, heavy rains may cause lead in surface soil to migrate into groundwater and eventually into water systems. Lead and lead compounds have been found at more than half of the sites on the National Priorities List (NPL) of hazardous waste sites in the United States, although this number may change as more sites are evaluated by the EPA. There are also approximately 400 Superfund sites contaminated with elevated (above background) levels of lead. Probability of Exposure Given the widespread distribution of lead in the environment, everyone has a low background level of around 1.66 ug/dL (CDC, 2003). For adults the major pathways for lead exposure are largely inhalation of lead-containing dusts and fumes in occupational settings, particularly mining, smelting and refining operations or battery manufacturing and reclamation operations (Gittleman et al., 1994). Exposure to lead may also occur through drinking water contaminated with lead leached from lead-containing pipes and fixtures. For children, ingestion of lead-containing dust and paint chips remain the primary routes of exposure (Juberg, 2000; Bornschein et al., 1986). The Third NHANES, phase 2 (1991-1994) measured blood lead levels in the US population and found that the US average for blood lead (BLL) was 2.9 µg/dL. For children 1-2 years of age, the most recent data show that the mean level is 3.1 µg/dL, all well below the CDC’s action level of 10 µg/dL (Brody et al., 1994). This report also identified subpopulations who were at increased risk of lead exposure as nonHispanic blacks or Mexican-American children aged 1-5 years, from lower-income families living in metropolitan areas with a population over 1 million, or living in older housing (MMWR, 1997). The risk for a BBL greater than or equal to 10ug/dl was higher among non-Hispanic black children living in housing built before 1946 (21.9%) or built during 1946-1973 (13.7%), among children in low-income households who lived in housing built before 1946 (16.4%) and among children in areas with populations greater than or equal to 1 million who live in housing built before 1946 (11.5%) when compared to children in other categories. The Second National Report on Environmental Exposures, using the 1999-2000 NHANES data, found an over all decrease in BLL for the US population, 1.66 ug/dL (CDC, 2003). The highest levels, however were still found in children aged 1-5 years (2.7ug/dL), and 2.2% of those children had BLLs greater or equal to 10ug/dL. As in the previous NHANES, higher prevalences of elevated BLLs in US children occurred in urban settings, lower socioeconomic groups, and immigrants. Health Effects In adults, lead adversely affects the nervous system at both high and low levels, the hematopoetic system and the reproductive system (reviewed in Juberg 2000). Lead poisoning can cause irritability, poor muscle coordination, and nerve damage. It has been associated with kidney disease (Goyer, 1971) with chronic and excessive lead exposure progressing to end-stage renal disease (Weeden, 1992). Lead exposure has been associated with increased blood pressure (Hertz-Picciotto and Croft, 1993), hearing and vision impairment, and reproductive problems (ATSDR, 1999,reviewed in Juberg, 2000). In children, lead poisoning can cause brain damage, mental retardation, behavioral problems, anemia, liver and kidney damage, hearing loss, hyperactivity, developmental delays, other physical and mental problems, and in extreme cases, death (Ernhart, 1992; reviewed in Juberg, 2000). Neurological effects including IQ deficits and in utero effects can occur at BBLs as low as 10ug/dl; hearing deficits at 20 ug/dl;

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and peripheral neuropathy at 40 ug/dl (reviewed in Juberg, 2000). Hematological problems begin at 10 ug/dl and renal problems start at less than 30 ug/dl. Children with even very low blood lead levels, below current CDC Guidelines, show poorer performance on tests of arithmetic skills, reading skills, nonverbal reasoning and short term memory (Lanphear et al., 2000). In a recent study of 240 children enrolled between 5 and 7 months for an unrelated study (Canfield et al., 2003). BLLs were obtained at 6, 12, 18, 24, 36, 48, and 60 months of age. BLL was inversely and significantly associated with IQ, with each increase of 10 µg per deciliter in the lifetime average blood lead concentration was associated with a 4.6-point decrease in IQ (P=0.004). Of greater concern was the finding that for the subsample of 101 children whose maximal lead concentrations remained below 10µg/dl, the change in IQ associated with a given change in lead concentration was greater than those children whose BLL were above 10ug/dl. IQ declined by 7.4 points as lifetime average BLLs increased from 1 to 10 µg/dl. During 2001 as many as twenty percent of Michigan's children under age six were lead poisoned in some urban neighborhoods (Kent, 2001). Over 4700 Michigan children were lead poisoned and an additional 20,000 were found to have damaging blood lead levels of 5 to 9 ug/dl (MDCH, 2001). The total annual economic costs of childhood lead poisoning in Michigan could be some $1.4 billion (based on Michigan's portion of national economic cost estimates). Alone, Michigan’s annual special education costs for the approximately 50 severely lead poisoned children, who require chelation therapy each year, are approximately $10 million (MDCH, 2002). Severity of Effects Although lead is an established carcinogen in experimental animals, it is classified only as a possible carcinogen in humans (IARC, 1987). Several epidemiological studies on cohorts of highly exposed workers have found only weak evidence of increased cancer mortality (Steenland and Bofetta, 2000). A recent study on the general US population found no association between BLL and increased risk of cancer (Jemal et al., 2002). Why Lead should be biomonitored in Michigan: • Lead is a neurotoxicant with adverse effects in children observed below 10ug/dl. • Children living in urban areas, with lower socioeconomic status are at increased risk of exposure to high levels of lead • According to Detroit Health Department and the Census, 73.9% of the City's housing was built before 1955 and, therefore, contains paint with a high proportion of lead. All children in the City of Detroit are considered at-risk by the State (Wayne State University, 2002-2003). • The cost to Michigan for treatment of lead-poisoned children is in the millions of dollars annually. References 1. Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological Profile for Lead [Update]. Atlanta, GA: Agency for Toxic Substances and Disease Registry; US Department of Health and Human Services; 1999 2. Bornschein RL, Succop PA, Krafft K M, Clark CS, Peace B and Hammond PB. Exterior surface dust lead, interior house dust lead and childhood lead exposure in an urban environment. In: Trace substances in environmental health. (Hemphill DD, ed.). 1986 University of Missouri. Columbia, MO 3. Brody, DJ, Prikle JL, Kramer RA, Flegal KM, Matte TD et al., Blood lead levels in the US population. Phase I of the Third National Health and Nutrition Examination Survey (NHANES III, 1998 to 1991). JAMA 1994;272:277-283. 4. Canfield RL, Henderson, Jr. CR, Cory-Slechta DA, Cox CC, Jusko TA, and Lanphear BP. Intellectual impairment in children with blood lead concentrations below 10 µg per deciliter. N Eng J Med 2003; 348:1517-1526. 5. Center for Disease Control and Prevention (CDC). Second National Report on Human Exposure to Environmental Chemicals. Results: Lead. 2003. US Center for Disease Control and Prevention.

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6. Detroit Lead Data. Wane State University college of Urban, Labor, and Metropolitan Affairs. 20022003. URL: http://www.detroitleadwsudata.org. 7. Ernhart CB. A critical review of low-level prenatal lead exposure in the human: effects of the fetus and newborn. Reprod Toxicol. 1992;6:9-40. 8. Finkelstein Y, Markowitz ME, Rosen JF. Low-level lead-induced neurotoxicity in children: an update on central nervous system effects. Brain Res Brain Rev 1998; 27:168-176. 9. Gittleman JL, Engelgau MM, Shaw J, Wille KK and Seigman PJ. Lead poisoning among battery reclamation workers in Alabama. J Occup Med 1994;36:526-532. 10. Goyer RA. Lad and the kidney. Current topics in pathology. 1971;55:147-176. 11. Hertz-Picciotto I and Croft J. Review of the relation between blood lead and blood pressure. Epid Rev 1993;15:352-373. 12. IARC. Lead and lead compounds. IARC Monogr Eval Carcinog Risk Hum 1987;23:325-415. 13. Jemal A, Graubard BL, Sevesa SS, Flegal KM. The association of blood lead level and cancer mortality among whites in the United States. Environ Health Perspect 2002;110:325-329. 14. Juberg DL. Lead and human health: an update. American Council on Science and Health 2000. 15. Kent County Health Department, Unpublished 2001 Datafile. 16. Lanphear BP et al. Cognitive Deficits Associated with Blood Lead Concentrations